miRNAs Modulate the Dichotomy of Cisplatin Resistance or Sensitivity in Breast Cancer: An Update of Therapeutic Implications

Cisplatin has a broad-spectrum antitumor activity and is widely used for the treatment of various malignant tumors. However, acquired or intrinsic resistance of cisplatin is a major problem for patients during the therapy. Recently, it has been reported Cancer Stem Cell (CSC)-derived drug resistance is a great challenge of tumor development and recurrence; therefore, the sensitivity of Breast Cancer Stem Cells (BCSCs) to cisplatin is of particular importance. Increasing evidence has shown that there is a relationship between cisplatin resistance/sensitivity genes and related miRNAs. It is known that dysregulation of relevant miRNAs plays a critical role in regulating target genes of cisplatin resistance/sensitivity in various pathways such as cellular uptake/efflux, Epithelial-Mesenchymal Transition (EMT), hypoxia, and apoptosis. Furthermore, the efficacy of the current chemotherapeutic drugs, including cisplatin, for providing personalized medicine, can be improved by controlling the expression of miRNAs. Thus, potential targeting of miRNAs can lead to miRNA-based therapies, which will help overcome drug resistance and develop more effective personalized anti-cancer and co treatment strategies in breast cancer. In this review, we summarized the general understandings of miRNAregulated biological processes in breast cancer, particularly focused on the role of miRNA in cisplatin resistance/sensitivity.

Automated summary

Cisplatin is widely used for treating malignant tumors but resistance remains a major challenge. Recent studies highlight the importance of Cancer Stem Cell (CSC)-derived drug resistance, particularly in Breast Cancer Stem Cells (BCSCs) when it comes to cisplatin sensitivity. Understanding the role of miRNAs in regulating cisplatin resistance/sensitivity can lead to more effective personalized anti-cancer therapies.